Epinephrine produces chronotropic effects on the electrical activity of Purkinje fibers by steepening the pacemaker depolarization, and by altering the level and duration of the action potential plateau. Previous experiments--using phosphodiesterase inhibitors and cyclic AMP derivatives--suggested that cyclic AMP may mediate at least some of epinephrine's actions. Further evidence will be obtained through new and more direct methods for introducing cyclic AMP intracellularly. The ionic basis of the epinephrine effects will be studied by using a voltage-clamp technique to dissect to various current components. The analysis of the results will be simplified pharmacologically, by developing selective inhibitors of individual components. Such pharmacological techniques will simplify the study of the outward currents which underly the plateau and pacemaker potential, and their sensitivity to external calcium concentration. A possible interrelationship between the actions of epinephrine and calcium ions will be explored. Finally, experiments will study the ionic nature and structural location of the outward plateau current which triggers the action potential repolarization. This component is strikingly augmented by epinephrine or monobutyryl cyclic AMP. The characterization of these effects will help clarify the mechanisms through which intracellular cyclic AMP modifies membrane permeability.